Dickstein G, Shechner C, Adawi F, Kaplan J, Baron E, Ish-Shalom S
Division of Endocrinology, Haifa Medical Center, Bnai Zion, Haifa, Israel.
Am J Med. 1997 May;102(5):454-8. doi: 10.1016/S0002-9343(97)00047-8.
Amiodarone hydrochloride is an iodine-rich drug effective in the control of various tachyarrhythmias. It is known to cause refractory to thyrotoxicosis, which usually does not respond to regular antithyroid drugs. Lithium bicarbonate is a medication used to treat psychiatric disorders; it also influences thyroid production and release of hormones. We tried it in combination with propylthiouracil (PTU) for the treatment of amiodarone-induced thyrotoxicosis.
Twenty-one patients were studied. The first group (n = 5) was treated by amiodarone withdrawal only. The second group (n = 7) received PTU (300 to 600 mg), and the third (n = 9) PTU (300 mg) and lithium (900 to 1350 mg) daily. Patient selection was not randomized. The PTU + lithium group had more severe symptoms and signs of thyrotoxicosis, as well as thyroxine levels at least 50% above the upper limit of normal. They also had been on a longer course of amiodarone treatment (34.3 +/- 11.9 months) than the PTU-only (11.4 +/- 7.5) and the no-treatment (7.8 +/- 4.2) groups.
While there was no difference between the first two groups in time until recovery (10.6 +/- 4.0 versus 11.6 +/- 0.5 weeks, respectively), the group receiving lithium normalized their thyroid function tests in only 4.3 +/- 0.5 weeks (P < 0.01 versus both other groups). T3 levels normalized even earlier-by 3 weeks of lithium treatment. No adverse effects of lithium were encountered, and the medication was stopped 4 to 6 weeks after achieving a normal clinical and biochemical state.
We conclude that lithium is a useful and safe medication for treatment of iodine-induced thyrotoxicosis caused by amiodarone. We would reserve this treatment for severe cases only. Further studies are needed to find out whether in patients with this troublesome complication lithium therapy could permit continuation of amiodarone treatment.
盐酸胺碘酮是一种富含碘的药物,对控制各种快速性心律失常有效。已知它会导致难治性甲状腺毒症,通常对常规抗甲状腺药物无反应。碳酸氢锂是一种用于治疗精神疾病的药物;它也会影响甲状腺激素的产生和释放。我们尝试将其与丙硫氧嘧啶(PTU)联合用于治疗胺碘酮所致的甲状腺毒症。
对21例患者进行了研究。第一组(n = 5)仅通过停用胺碘酮进行治疗。第二组(n = 7)接受PTU(300至600毫克),第三组(n = 9)每日接受PTU(300毫克)和锂(900至1350毫克)。患者选择未采用随机分组。PTU + 锂组甲状腺毒症的症状和体征更严重,甲状腺素水平至少比正常上限高50%。他们接受胺碘酮治疗的疗程(34.3 +/- 11.9个月)也比仅接受PTU治疗的组(11.4 +/- 7.5个月)和未治疗组(7.8 +/- 4.2个月)更长。
前两组直至恢复的时间无差异(分别为10.6 +/- 4.0周和11.6 +/- 0.5周),而接受锂治疗的组仅在4.3 +/- 0.5周时甲状腺功能检查恢复正常(与其他两组相比,P < 0.01)。T3水平恢复正常的时间更早——锂治疗3周后。未出现锂的不良反应,在临床和生化状态恢复正常后4至6周停用该药物。
我们得出结论,锂是治疗胺碘酮所致碘性甲状腺毒症的一种有用且安全的药物。我们仅会将这种治疗方法用于严重病例。需要进一步研究以确定在患有这种麻烦并发症的患者中,锂疗法是否能允许继续使用胺碘酮治疗。